Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A young man who had had two episodes of high-altitude pulmonary edema in the absence of any respiratroy distress was noted to have a depression of his hypoxic and hypercapnic ventilatory drives. It is postulated that because of his blunted ventilaory drives, the patient progessed to coma on exposure to low ambient oxygen tensions (i.e., high altitude) without ever increasing his ventilation. The importance of including highaltitude pulmonary edema in the differential diagnosis of any patient who is admitted with coma after a sojourn at high altitude is stressed.
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PMID:Recurrent high altitude pulmonary edema with blunted chemosensitivity. 113 51

Effects of high altitude hypoxia on systolic time intervals were examined in 34 healthy men: 20 sea level residents studied at rest and at the end of 3 minutes steady isometric (handgrip) exercise at sea level and then serially for the first 5 days and on the tenth day, at an altitude of 3658 m, and I4 permanent residents at high altitude studied at high altitude. In the sea level residents there was a significant increase in the pre-ejection period (PEP), abbreviation of the left ventricular ejection time (LVET), both corrected for heart rate, and prolongation of the PEP/LVET ratio at high altitude. The maximum changes were seen on days 2 and 3; these parameters tended to approach sea level control values by the tenth day. The systolic time interval values of high altitude residents were similar to the control values of the sea level residents obtained at sea level but significantly different from the changes in the sea level values seen in the first 4 days at high altitude. It thus appears that while the high altitude residents do not show any left ventricular dysfunction as determined by systolic time intervals, healthy sea level residents when exposed to high altitude hypoxia show a significant depression of the left ventricular function for at least the first 4 days. This might be a contributing factor in the genesis of high altitude pulmonary oedema.
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PMID:Effects of high altitude hypoxia on left ventricular systolic time intervals in man. 113 31

It is reported on the results of the treatment with artificial ventilation in 20 patients with complicated myocardial infarction. As indicating sign a decreased arterial PO2 (lower than 70 Torr at an respiration of 50% O2 in the respiration air) was considered. Further references to clinical indications were depression of the breathing centre, severe pulmonary oedema, shock and life-threatening therapy-resistent disturbances of the rhythm. The long-term successes of the treatment with controlled respiration showed a clear dependence on the severity of the cardiac lesion and the general condition of the patient. In 10 cases only a transient improvement could be achieved. Three patients survived.
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PMID:[The clinical significance of controlled artificial respiration in patients with acute myocardial infarct]. 119 86

To investigate the role of hypoxic ventilatory response (HVR) in the pathogenesis of acute mountain sickness (AMS) and high-altitude pulmonary edema (HAPE), we performed two studies. In the first study, nine healthy male lowlanders were exposed to a simulated altitude of 3,700 m (485 Torr) for 24 h in a hypobaric chamber. Subjects (n = 4) with lower alveolar ventilation on arrival at 3,700 m subsequently developed more severe AMS 24 h after the exposure. The relative hypoventilation was related to the lower HVR measured at low altitude, suggesting a possible role of low HVR in AMS. In the second study nine lowlanders with a previous history of HAPE (HAPE-S) and six control subjects were exposed to a simulated altitude of 3,200 m (515 Torr). At low altitude, HVR (delta VE/delta SaO2) in HAPE-S was significantly lower than that of controls (-0.40 +/- 0.20 vs. -0.85 +/- 0.21 L/min/%, p < 0.01). At high altitude HAPE-S showed lower PaO2, higher PaCO2 and lower PAO2, compared with controls, i.e., relative hypoventilation. In one of the HAPE-S, who showed the lowest PaO2 at the simulated altitude, oxygen breathing resulted in a paradoxical increase in ventilation, suggesting hypoxic ventilatory depression. These two studies suggest that low HVR may a contributing rather than a critical factor in the pathogenesis of AMS and HAPE.
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PMID:[Exposure to high altitude: ventilatory control in relation to syndromes of high altitude]. 130 17

Of 113 methyl isocyanate (MIC)-exposed subjects studied initially at Bhopal, India, 79, 56, 68, and 87 were followed with clinical, lung function, radiographic, and immunologic tests at 3, 6, 12, 18, and 24 months. Though our cohort consisted of subjects at all ages showing a varied severity of initial illness, fewer females and young subjects were seen. Initially all had eye problems, but dominant symptoms were exertional dyspnea, cough, chest pain, sputum, and muscle weakness. A large number showed persistent depression mixed with anxiety, with disturbances of personality parameters. The early radiographic changes were lung edema, overinflation, enlarged heart, pleural scars, and consolidation. The persistent changes seen were interstitial deposits. Lung functions showed mainly restrictive changes with small airway obstruction; there was impairment of oxygen exchange. Oxygen exchange improved at 3-6 months, and spirometry improved at 12 months, only to decline later. The expiratory flow rates pertaining to large and medium airway function improved, but those for small airways remained low. There were changes of alveolitis in bronchoalveolar lavage fluid on fiber optic bronchoscopy, and in 11 cases positive MIC-specific antibodies to IgM, IgG, and IgE were demonstrated. On follow up, only 48% of the subjects were clinically stable, while 50% showed fluctuations. Thirty-two percent of the subjects had lung function fluctuations. Detailed sequential behavior over 2-4 years was predicted for dyspnea, forced vital capacity, maximum expiratory flow rate (0.25-0.75), peak expiratory flow rate, VO2, and depression score. A model for clinical behavior explained a total variance of 52.4% by using the factors of cough, PCO2 and X-ray zones in addition to above five parameters. The behavior of the railway colony group (1640 patients) revealed a similar pattern of illness. When this observed pattern of changes was transferred to the affected Bhopal city sections (with an equitable age-sex distribution), our model results were again validated. Thus the picture of MIC-induced disease seems similar despite the differences for age-sex and initial severity of illness in our cohort and in the population of Bhopal city as predicted by our model.
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PMID:Sequential respiratory, psychologic, and immunologic studies in relation to methyl isocyanate exposure over two years with model development. 139 63

A 63 year old female, who was admitted to a psychiatric hospital for schizophrenia, was referred to our emergency room because of sudden loss of consciousness and convulsions. On arrival, she was drowsy and hypoxemic. Her chest X-ray showed cardiomegaly with pulmonary edema. ECG showed marked ST depression in precordial leads and serum chemistry revealed marked elevation of CPK, GOT and LDH along with hyponatremia and hypochloremia. She was immediately admitted to CCU on suspicion of acute non-transmural myocardial infarction complicated with congestive heart failure. After fluid restriction and intravenous infusion of dopamine she passed large amount of urine, and her consciousness level, electrolyte imbalance and ECG change, improved gradually. Although serum CPK level increased as high as 32,307 IU/ml, there were no signs of left ventricular asynergy on UCG and CPK isozyme analysis performed later revealed more than 99% of serum cCPK was MM-type. We concluded that water intoxication was the cause of the ECG change and the elevated serum CPK, GOT and LDH levels. There are few reports on elevated CPK level in association with water intoxication, in which rhabdomyolysis is speculated as the cause of CPK elevation. But there is no report on ECG change complicated with water intoxication. In our case, electrolyte imbalance caused by water intoxication seemed to play a major role in ST depression and QT prolongation. Although water intoxication is a rare disorder in the general population, it is not infrequent among patients with psychiatric diseases. Care must be taken when such patients present ECG change and serum enzyme elevation mimicking ischemic heart disease.
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PMID:[A water intoxication patient who showed remarkable ST depression and suspected ischemic heart disease]. 152 80

Clinical characteristics and therapeutic problems of neurogenic pulmonary edema (NPE) occurring in the acute stage of severe subarachnoid hemorrhage (SAH) were examined. The relationship between SAH and NPE was studied in 208 patients who arrived at the hospital in the acute stage (within 24 hours after the onset) of severe SAH in the past nine years. NPE was observed in four (6%) of 64 Grade III patients, nine (18%) of 49 Grade IV patients and 20 (21%) of 95 Grade V patients. Higher grade patients tended to be complicated by NPE more frequently. CT findings of these 33 patients with NPE belonged to Fisher's Group 3 or 4 (23 of 110 group-3 patients and 10 of 88 group-4 patients). Concerning ECG abnormalities, depression of ST segment, abnormal T waves, sinus tachycardia, and right bundle-branch block were observed more frequently in the NPE group than in the non-NPE group. In comparison of the age, blood pressure, PaO2, serum electrolyte, WBC, and blood sugar level on admission between the two groups, significantly higher values of diastolic pressure and blood sugar levels were shown in the NPE group than non-NPE group. The mean interval between the onset of SAH and the diagnosis of NPE on chest film was 2.5 hours, while the NPE findings disappeared within three days after the onset of SAH (mean 1.2 days). In all cases, the NPE findings disappeared after a variety of respiratory managements had been carried out.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical evaluation of neurogenic pulmonary edema following acute stage of subarachnoid hemorrhage]. 157 64

Ventilatory depression and apnea are well-known early pulmonary responses of sepsis in infants, yet their underlying mechanisms are not understood. To further elucidate the pathophysiology, we induced Escherichia coli septicemia in piglets and studied the sequential changes in intrapulmonary shunt (QS/QT), physiological dead space (VD/VT), minute ventilation (VE), and blood gases for up to 6 hours of lethal sepsis. Lung lymph was also collected and extravascular lung water (EVLW) was measured. Histology confirmed that interstitial edema developed 1 hour after E. coli infusion. These data suggest that high permeability pulmonary edema and hypoxemia following early intrapulmonary shunt increase may be the causes of septic ventilatory depression.
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PMID:[An experimental study on the pathophysiology of septic ventilatory depression]. 165 Jun 39

Disturbances in lipid metabolism have been observed during the early phase of acute myocardial ischemia. Accumulation of fatty acids in and around the ischemic cardiac cells has been implicated to play a role in both contractile and electrophysiological abnormalities. Linolenic acid is an essential fatty acid and constitutes the phospholipid moiety of the cell membrane. The purpose of this work was to study the effects of linolenic acid on the heart using canine preparations. A direct left atrial injection was used as the route of administration because intravenous injections of linolenic acid inevitably cause pulmonary edema. A surface lead electrocardiogram (ECG), an epicardial electrogram, femoral arterial pressure, left ventricular pressure and its time derivative (dp/dt) were recorded before and after drug administration. Various dosages of linolenic acid (1 mg, 5 mg, 10 mg, 20 mg, 30 mg and 60 mg/kg) and a control buffer solution were tested. The results showed that linolenic acid has a potent dose-dependent bradycardic and myocardial depression effect starting from a dose of 5 mg/kg (delta HR = -20.1 +/- 4.0 bpm, delta dp/dt = 364.3 +/- 66.0 mmHg, sec-1, p less than 0.01 vs. control). At a high dose of 30 mg/kg, linolenic acid induced premature ventricular complexes. Furthermore, ventricular tachycardia was observed in 5 of the 8 dogs (62.5%) receiving the high dose of 60 mg/kg. We conclude that linolenic acid has profound effects on the canine heart; at a low dose, it causes bradycardia and myocardial depression, while at a high dose, it also produces ventricular irritability.
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PMID:Effects of linolenic acid on the canine heart. 168 Sep 97

The safety of prehospital pharmacologic therapy has not been well studied. The authors evaluated field use of morphine sulfate (MS) in San Francisco County over a 6-month period. Paramedics assessed patients for ischemic chest pain (ICP) and/or pulmonary edema (PE), made base hospital contact, and administered 2- to 4-mg doses of intravenous morphine according to treatment protocols. Clinical assessments and patient responses to therapy were recorded by both field paramedics and emergency department (ED) physicians. Safety was evaluated by determining the (1) accuracy of paramedic field assessment, (2) appropriateness of field administration of MS, and (3) therapeutic complications. During the study period, paramedics administered MS to 84 patients. In 69 cases paramedic assessment of either ICP and/or PE corresponded to ED physician diagnosis. In five cases paramedics correctly recognized ICP but missed physical findings of PE. In this group the paramedics' assessment was considered inaccurate but the judgement to give MS was considered appropriate. In the remaining 10 cases paramedics identified ICP or PE but the ED physician diagnosed a different condition. These assessments were considered inaccurate and the management inappropriate. Therefore, overall paramedic accuracy was 77% (true rate 73% to 82%, 95% confidence interval); appropriateness of therapy was 88% (true rate 85% to 92%, 95% confidence interval); and the overall complication rate was 6% (true rate 2% to 12%, 95% confidence interval). Complications of respiratory depression or hypotension occurred in only one of the cases in which MS was inappropriately administered.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Safety of pre-hospital therapy with morphine sulfate. 173 17


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